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1. Enhancing innate immunity against virus in times of COVID-19: trying to untangle facts from fictions

Author

Alan Estrada-Cardona, María Isabel Rojo-Gutiérrez, Désirée Larenas-Linnemann, César Fireth Pozo-Beltrán, Ernesto Onuma-Takane, Blanca Estela Del Río-Navarro, María Virginia Blandón-Vijil, Jorge A. Luna-Pech, J. E. Gereda, Noel Rodríguez-Pérez, Alfredo Arias-Cruz, and Elsy Maureen Navarrete-Rodríguez

Subjects
BV, Bacterial vaccine, mindfulness, ACE2, Angiotensin converting enzime-2, Systemic inflammatory response syndrome, TCR :T-cell receptor, APC, Antigen-presenting cell, Heat shock proteins, HLA-DR, bacterial vaccine, Immunoglobulin, IGFBP6, immune response, DLE, Dialyzable leukocyte extract, PPD, Purified protein derivative (tuberculin), trained immunity, MCP-1, Monocyte chemoattractant protein-1, NK, Natural killer, Gαs: G protein coupled receptor alfa-subunits, HSP, Rapid eye movement, RIPK2, Pandemic, Immunology and Allergy, TNF-α, Tumor necrosis factor alpha, R0 : Basic reproduction number, REM, PUFA, Polyunsaturated fatty acid, NOD2, Nucleotide-binding oligomerization domain-containing protein 2, Toll-like receptor, Reactive oxygen species, SARS-CoV-2, Respiratory tract infections, exercise, CNS, Central nervous system, Interferon, IG, MMR, DC, Dendritic cell, Bacterial vaccine, Reactive nitrogen species, ROS, PKC, Protein kinase C, BCG, Bacillus Calmette-Guérin, DAMPs, Damage-associated molecular patterns, TLR, Toll-like receptor, Pulmonary and Respiratory Medicine, lcsh:Immunologic diseases. Allergy, medicine.medical_specialty, Interleukin, MBSR, CCL-5, Chemokine (C-C motif) ligand 5, Immunology, Insulin-like growth-factor-binding-protein 6, IL, Major histocompatibility complex class II cell surface receptor, ICAM-1, COVID-19, Coronavirus disease-2019, Article, OxPhos: Oxidative phosphorylation, PAMPs, Immune system, Immunity, NK-cell, URTI, Upper-respiratory tract infection, Bacillus Calmette-Guérin, medicine, innate, Intercellular adhesion molecule type 1, IFN, MODS, Multi-organ dysfunction syndrome, NF-κB, Nuclear factor kappaB, sleep, Intensive care medicine, Innate immune system, Severe acute respiratory syndrome coronavirus 2, SIRS, business.industry, CI, Confidence interval, Pathogen-associated molecular patterns, PBMC, COVID-19, Mindfulness-based stress reduction, mCa++: Intramitochondrial calcium, Review article, MyD88, Myeloid differentiation primary response 88, TRPV, Thermolabile calcium channels, CXCR3A, CXC chemokine receptor 3A, Receptor iteracting serine/threonine kinase 2, RNA, Ribonucleic acid, RNS, business, lcsh:RC581-607, Peripheral blood mononuclear cell, PI3K/Akt: Phosphatidylinositol 3-kinase pathway, OR, Odds ratio, Th, T helper-cell
Abstract

Introduction In light of the current COVID-19 pandemic, during which the world is confronted with a new, highly contagious virus that suppresses innate immunity as one of its initial virulence mechanisms, thus escaping from first-line human defense mechanisms, enhancing innate immunity seems a good preventive strategy. Methods Without the intention to write an official systematic review, but more to give an overview of possible strategies, in this review article we discuss several interventions that might stimulate innate immunity and thus our defense against (viral) respiratory tract infections. Some of these interventions can also stimulate the adaptive T- and B-cell responses, but our main focus is on the innate part of immunity. We divide the reviewed interventions into: 1) lifestyle related (exercise, >7 h sleep, forest walking, meditation/mindfulness, vitamin supplementation); 2) Non-specific immune stimulants (letting fever advance, bacterial vaccines, probiotics, dialyzable leukocyte extract, pidotimod), and 3) specific vaccines with heterologous effect (BCG vaccine, mumps-measles-rubeola vaccine, etc). Results For each of these interventions we briefly comment on their definition, possible mechanisms and evidence of clinical efficacy or lack of it, especially focusing on respiratory tract infections, viral infections, and eventually a reduced mortality in severe respiratory infections in the intensive care unit. At the end, a summary table demonstrates the best trials supporting (or not) clinical evidence. Conclusion Several interventions have some degree of evidence for enhancing the innate immune response and thus conveying possible benefit, but specific trials in COVID-19 should be conducted to support solid recommendations.

Published
2020

2. Drug repurposing of anti-infective clinical drugs: Discovery of two potential anti-cytokine storm agents

Author

Da-gui Chen, Ye Tu, De-pei Kong, Zhibin Wang, Su Li, Chen-xi Zhang, Chunlin Zhuang, and Wannian Zhang

Subjects
0301 basic medicine, Lipopolysaccharides, Male, Imipenem, Imipenem: PubChem CID 104838, MERS, Middle East Respiratory Syndrome, Drug repurposing, Cytokine storm, hPBMC, human peripheral blood mononuclear cell, Mice, 0302 clinical medicine, IC50, half-maximal inhibitory concentration, BALF, bronchoalveolar lavage fluid, Medicine, CXCL1, CXC chemokine ligand 1, media_common, COVID-19, coronavirus disease 2019, General Medicine, Entecavir, NLRP3, NLR family PYRIN domain containing-3, CSS, cytokine storm syndrome, Interleukin-10, Drug repositioning, 030220 oncology & carcinogenesis, LPS, lipopolysaccharide, Cytokines, G-CSF, granulocyte-colony stimulating factor, Coronavirus Infections, Cytokine Release Syndrome, medicine.drug, Drug, Guanine, media_common.quotation_subject, Acute Lung Injury, Pneumonia, Viral, RM1-950, Lung injury, Peripheral blood mononuclear cell, Article, Proinflammatory cytokine, 03 medical and health sciences, MCP-1, monocyte chemoattractant protein -1, Anti-inflammation, Animals, Humans, Pandemics, ARDS, acute respiratory distress syndrome, ComputingMethodologies_COMPUTERGRAPHICS, Pharmacology, MIP-1α, macrophage inflammatory protein 1 alpha, Entercavir: PubChem CID 135398508, SARS-CoV-2, Severe Acute Respiratory Syndrome Coronavirus -2, business.industry, Tumor Necrosis Factor-alpha, Macrophages, Drug Repositioning, COVID-19, medicine.disease, IL, interleukin, COVID-19 Drug Treatment, Mice, Inbred C57BL, FDA, U.S. Food and Drug Administration, 030104 developmental biology, Immunology, Leukocytes, Mononuclear, CCL-5, chemokine (C-C motif) ligand 5, Therapeutics. Pharmacology, business, IP10, interferon-γ-inducible protein 10
Abstract

Graphical abstract, Highlights • Entecavir and imipenem alleviated LPS-induced cytokine storm syndrome. • Entecavir and imipenem mitigated LPS-induced acute lung injury. • Entecavir and imipenem inhibited LPS-stimulated TNF-α and IL-10 in hPBMC. • Entecavir and imipenem attenuated LPS-activated NF-κB., Coronavirus Disease 2019 (COVID-19) caused by Severe Acute Respiratory Syndrome Coronavirus -2 (SARS-CoV-2) has been widely spread in the world with a high mortality. Cytokine storm syndrome (CSS) and acute lung injury caused by SARS-CoV-2 infection severely threaten the patients. With the purpose to find effective and low-toxic drugs to mitigate CSS, entecavir and imipenem were identified to reduce TNF-α using a LPS-induced macrophage model from the anti-infective drug library. Entecavir and imipenem efficiently suppressed the release of inflammatory cytokines by partly intervention of NF-κB activity. The acute lung injury was also alleviated and the survival time was prolonged in mice. In addition, entecavir and imipenem inhibited the release of TNF-α and IL-10 in human peripheral blood mononuclear cells (hPBMCs). Collectively, we proposed that entecavir and imipenem might be candidates for the treatment of CSS.

Published
2020

3. Enhancing innate immunity against virus in times of COVID-19: Trying to untangle facts from fictions.

Author

Larenas-Linnemann D, Rodríguez-Pérez N, Arias-Cruz A, Blandón-Vijil MV, Del Río-Navarro BE, Estrada-Cardona A, Gereda JE, Luna-Pech JA, Navarrete-Rodríguez EM, Onuma-Takane E, Pozo-Beltrán CF, and Rojo-Gutiérrez MI

Abstract

Introduction: In light of the current COVID-19 pandemic, during which the world is confronted with a new, highly contagious virus that suppresses innate immunity as one of its initial virulence mechanisms, thus escaping from first-line human defense mechanisms, enhancing innate immunity seems a good preventive strategy., Methods: Without the intention to write an official systematic review, but more to give an overview of possible strategies, in this review article we discuss several interventions that might stimulate innate immunity and thus our defense against (viral) respiratory tract infections. Some of these interventions can also stimulate the adaptive T- and B-cell responses, but our main focus is on the innate part of immunity. We divide the reviewed interventions into: 1) lifestyle related (exercise, >7 h sleep, forest walking, meditation/mindfulness, vitamin supplementation); 2) Non-specific immune stimulants (letting fever advance, bacterial vaccines, probiotics, dialyzable leukocyte extract, pidotimod), and 3) specific vaccines with heterologous effect (BCG vaccine, mumps-measles-rubeola vaccine, etc)., Results: For each of these interventions we briefly comment on their definition, possible mechanisms and evidence of clinical efficacy or lack of it, especially focusing on respiratory tract infections, viral infections, and eventually a reduced mortality in severe respiratory infections in the intensive care unit. At the end, a summary table demonstrates the best trials supporting (or not) clinical evidence., Conclusion: Several interventions have some degree of evidence for enhancing the innate immune response and thus conveying possible benefit, but specific trials in COVID-19 should be conducted to support solid recommendations., Competing Interests: All authors declared or they have no potential conflicts of interest. The following authors, indicated relations with the pharmaceutical industry: Dr. Larenas Linnemann reports personal fees from Allakos, Amstrong, Astrazeneca, Boehringer Ingelheim, Chiesi, DBV Technologies, Grunenthal, GSK, MEDA, Menarini, MSD, Novartis, Pfizer, Novartis, Sanofi, Siegfried, UCB, Alakos, Gossamer, grants from Sanofi, Astrazeneca, Novartis, UCB, GSK, TEVA, Boehringer Ingelheim, Chiesi, Purina institute., (© 2020 The Authors.)

Published
2020
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4. A TLR2/S100A9/CXCL-2 signaling network is necessary for neutrophil recruitment in acute and chronic liver injury in the mouse

Author

Anna, Moles, Lindsay, Murphy, Caroline L, Wilson, Jayashree Bagchi, Chakraborty, Christopher, Fox, Eek Joong, Park, Jelena, Mann, Fiona, Oakley, Rachel, Howarth, John, Brain, Steven, Masson, Michael, Karin, Ekihiro, Seki, and Derek A, Mann

Subjects
Male, ALD, alcoholic liver disease, ALT, alanine transaminase, S100A8, S100 calcium binding protein A8, S100A9, S100 calcium binding protein A9, NASH, non-alcoholic steatohepatitis, TLR, toll like receptor, Chemokine CXCL2, PCNA, proliferating cell nuclear antigen, Liver fibrosis, CCL-2, chemokine (C-C motif) ligand 2, TNF-α, tumor necrosis factor-α, Toll like receptor, α-SMA, α-smooth muscle actin, Mice, ROS, reactive oxygen species, LTA, lipoteichoic acid, CCl4, carbon tetrachloride, IL6, interleukin-6, Animals, Calgranulin B, Humans, Calgranulin A, CXCL-2, chemokine (C-X-C motif) ligand 2, AHH, acute alcoholic hepatitis, Carbon Tetrachloride, S100A9, Mice, Knockout, Inflammation, Wound Healing, Neutrophil, Toll-Like Receptor 2, Mice, Inbred C57BL, Toll-Like Receptor 4, Disease Models, Animal, CXCL-1, chemokine (C-X-C motif) ligand 1, PSC, primary sclerosing cholangitis, Neutrophil Infiltration, Chemical and Drug Induced Liver Injury, Chronic, APAP ALF, acetaminophen acute liver failure, CCL-5, chemokine (C-C motif) ligand 5, PBC, primary biliary cirrhosis, Chemical and Drug Induced Liver Injury, Leukocyte L1 Antigen Complex, IHC, immunohistochemistry, Signal Transduction, Research Article
Abstract

Background & Aims Neutrophils are important immune effectors required for sterile and non-sterile inflammatory responses. However, neutrophils are associated with pathology in drug-induced liver injury, acute alcoholic liver disease, and ischemia-reperfusion injury. An understanding of the complex mechanisms that control neutrophil recruitment to the injured liver is desirable for developing strategies aimed at limiting neutrophil-mediated cellular damage. Methods Wt, tlr2−/−, tlr4−/−, and s100a9−/− mice were administered CCl4 either acutely (8, 24, 48, or 72 h) or chronically (8 weeks) and livers investigated by histological (IHC for neutrophils, fibrogenesis, proliferation, and chemotactic proteins) or molecular approaches (qRT-PCR for neutrophil chemoattractant chemokines and cytokines as well as pro-fibrogenic genes). Results Mice lacking TLR2 or S100A9 failed to recruit neutrophils to the injured liver and had a defective hepatic induction of the neutrophil chemokine CXCL-2. Hierarchy between TLR2 and S100A9 proved to be complex. While induction of S100A9 was dependent on TLR2 in isolated neutrophils, there was a more complicated two-way signalling cross-talk between TLR2 and S100A9 in whole liver. However, wound-healing and regenerative responses of the liver were unaffected in these genetic backgrounds as well as in wild type mice, in which neutrophils were depleted by infusion of Ly-6G antibody. Conclusions We have identified TLR2 and S100A8/S100A9 as key regulators of hepatic CXCL-2 expression and neutrophil recruitment. This novel TLR2-S100A9-CXCL-2 pathway may be of use in development of new strategies for selectively manipulating neutrophils in liver disease without impairing normal wound healing and regenerative responses.

Published
2013

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